Over the past century, the average sleep duration of Americans has decreased by nearly 2 hours. Sleep curtailment in healthy young adults results in a series of alterations that are typical of human aging, including reduced glucose tolerance and/or insulin resistance, elevated evening cortisol levels, reduced leptin levels and increased sympathetic activity. These findings suggest that sleep loss may accelerate the development or increase the severity of age-related metabolic disorders, including obesity, hypertension and diabetes. Conversely, fulfilling sleep need at all ages may increase the likelihood of successful aging. A definition of sleep need has, however, remained elusive, but the stable total sleep time achieved after a prolonged period of extended bedtimes, i.e. sleep capacity, is a measurable variable that may be a functionally relevant substitute of sleep need Our preliminary data indicate that the amount and intensity of slow-wave sleep (SWS) play a major role in determining both the response to and the pattern of recovery from sleep loss and that there important age and gender differences in SWS regulation. These results predict that vulnerability to chronic partial sleep loss and the pattern of recovery from sleep loss will be age- and genderdependent. The specific aims of the present project are: therefore: 1. To test the hypothesis that sleep restriction is associated with alterations of glucose tolerance, endocrine profiles, cardiovascular function and neurobehavioral parameters in young (18-25 y), middle-aged (35-50 y) and older (60-75 y) healthy men and women. 2. To test the hypothesis that extending the bedtimes to allow for sleep recovery will reverse alterations resulting from sleep restriction in young, middle-aged and older men and women. 3. To test the hypothesis that there are age and gender differences in total amount of sleep recovered following sleep restriction. 4. To determine sleep capacity in young, middle-aged and older men and women and test the hypothesis that there are age and gender differences in sleep capacity. 5. To test the hypothesis that individual differences in sleep capacity are predicted by individual differences in markers of sleep-wake homeostasis (SWS and SW activity). 6. To test the hypothesis that the magnitude of alterations following sleep restriction is dependent on individual sleep capacity.